@Article{or.2022.028225,
AUTHOR = {YAN ZHUANG, CHUNLAN NING, PENGFEI LIU, YANPENG ZHAO, YUE LI, ZHENCHI MA, LULING SHAN, YINGZHE PIAO, PENG ZHAO, XUN JIN},
TITLE = {LSM12 facilitates the progression of colorectal cancer by activating the WNT/CTNNB1 signaling pathway},
JOURNAL = {Oncology Research},
VOLUME = {30},
YEAR = {2022},
NUMBER = {6},
PAGES = {289--300},
URL = {http://www.techscience.com/or/v30n6/51597},
ISSN = {1555-3906},
ABSTRACT = {Aberrant activation of the WNT signaling pathway is a joint event in colorectal cancer (CRC), but the molecular
mechanism is still unclear. Recently, RNA-splicing factor LSM12 (like-Sm protein 12) is highly expressed in CRC tissues.
This study aimed to verify whether LSM12 is involved in regulating CRC progression via regulating the WNT signaling
pathway. Here, we found that LSM12 is highly expressed in CRC patient-derived tissues and cells. LSM12 is involved in
the proliferation, invasion, and apoptosis of CRC cells, similar to the function of WNT signaling in CRC. Furthermore,
protein interaction simulation and biochemical experiments proved that LSM12 directly binds to CTNNB1 (also known
as β-Catenin) and regulates its protein stability to affect the CTTNB1-LEF1-TCF1 transcriptional complex formation and
the associated WNT downstream signaling pathway. LSM12 depletion in CRC cells decreased the in vivo tumor growth
through repression of cancer cell growth and acceleration of cancer cell apoptosis. Taken together, we suggest that the
high expression of LSM12 is a novel factor leading to aberrant WNT signaling activation, and that strategies targeting
this molecular mechanism may contribute to developing a new therapeutic method for CRC.},
DOI = {10.32604/or.2022.028225}
}